Heart rate and contractility

Question 1

The basics about cardiac muscle

Answer 1

• Myocardium
• Each cell (myofibril) is made up of hundreds of myofibrils, made up of filaments (actin, myosin)
• Remember the I and A bands and the Z disc and the role of Ca+2 in contraction

Question 2

Striated (skeletal) vs. cardiac muscle

Answer 2

• Better connected muscle cells – syncytium→action potential jumps quicker from one cell to the next. FASTER
• There ion exchange points (gap junctions) between cells allowing electrical coupling→all cells contract at the same time. IN SYNC
• The gap junctions are in the intercalated discs, a unique feature of cardiac muscle. DIFFERENT APPEARANCE
• Action potential is not from a motor neuron → AUTONOMOUS
• Action potential last longer (150ms vs. 2ms)→AVOID TETANY

Question 3

SAN

Answer 3

The heart contracts when stimulated by an electrical wave that comes from specialised muscle cells spontaneously in the area of the heart known as the sino-atrial node (SA Node) = pacemaker

Question 4

What is special about myocytes?

Answer 4

• Cardiac contractile (ventricular) cells have additional voltage gated K+ channels and Ca+2 special channels (allow Ca+2 from extracellular and K+ out). VG-Ca, VG-K or VG-Na
• Cardiac pacemaker cells have special spontaneous Na+ channels (FUNNY channels) instead of VG, which effectively is making them more sensitive to depolarization (i.e. contraction!)

Remember role of gap junctions and T tubules in the ion exchange process
• Ca+2 channels enable longer action potential compared to skeletal muscle - Ca+2 comes from the outside as well as the inside!

Question 5

What happens in the cardiac cells?

Answer 5

1. Pacemaker cells (atrial cells) depolarize to threshold leading to the impulse being propagated to contractile cells (ventricular cells) - every beat!

When transmitted to contractile cells the gap junctions allow synchrony and the special channels promote contraction of myocytes

Question 6

Factors affecting the heart rate (HR) are known as

Answer 6

chronotropic

Question 7

• Factors affecting heart contractility are known as

Answer 7

ionotropic

Question 8

HR regulation

Answer 8

• Initiated and maintained by the SAN and conducted by the cardiac conductive system
• Regulated by:
• Sympathetic/parasympathetic nervous system. It cannot start
or stop, but it can regulate the speed
• Hypothalamus and brainstem
• ”Emergency” contraction from AV node – but nowhere near as efficient or coordinated!
• Adrenal glands (adrenaline – same as NA path)
• BP and oxygenation needs
• Drugs that affect the Ca+2 channels or the VG channels
• Muscle changes – exercise or pathology!

Norepinephrine shortens the interval between action potentials increasing heart rate (PS, vagus nerve)
• Acetylcholine lengthens the interval, therefore decreasing the heart rate (S, sympathetic trunk)
• Adrenaline = same as NE
• AV node – arrythmias!
• Low BP (for example bleeding) → increases HR
• Low oxygenation (for example anaemia) → increases HR

Question 9

Contractility (inotropy)

Answer 9

• Physical changes in the fibers
• Sympathetic nervous system. NE can affect the non SAN myocytes increasing the strength of the contraction (through opening Ca+2 channels)
• Parasympathetic nervous system. ACo blocks the sympathetic action on ventricular myocytes (muscarinic cholinergic agonist effect)
• Other catecholamines (affect Ca+2 concentration)
• End diastolic pressure (preload), HR and SVR (or
afterload)
• Drugs that affect the Ca+2 channels or the VG channels